RB PHOSPHORYLATION IN SODIUM BUTYRATE-RESISTANT HL-60 CELLS - CROSS-RESISTANCE TO RETINOIC ACID BUT NOT VITAMIN-D3

被引:13
作者
YEN, A [1 ]
VARVAYANIS, S [1 ]
机构
[1] CORNELL UNIV,DEPT PATHOL,CANC BIOL LABS,ITHACA,NY 14853
关键词
D O I
10.1002/jcp.1041630310
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
To examine the potential coupling between inducible cellular changes in RE (retinoblastoma) tumor suppressor protein phosphorylation and ability to CO growth arrest and differentiate, HL-60 promyelocytic leukemia cells were cultured in incremental sodium butyrate (NaB) concentrations and thereby made resistant to the growth inhibitory effects of sodium butyrate, which normally induces GO arrest and monocytic differentiation in wild type HL-6O cells. The resistant cells were also unable to differentiate in response to NaB, indicating that a regulatory function controlling both GO growth arrest and differentiation had been affected. The induced resistance was not genetic in origin since the cells regained the ability to GO arrest and differentiate after being recultured in medium free of sodium butyrate for only three days. The resistant cells had similar cell cycle phase durations as the original wild type cells. The resistant cells retained the ability to both GO arrest and differentiate in response to 1,25-dihydroxy vitamin D3 (VD3), normally an inducer of GO arrest and monocytic differentiation in wild type cells. However, they were cross-resistant to retinoic acid (RA), another ligand for the same steroid thyroid hormone receptor family, which induces GO arrest and myeloid differentiation in wild type cells. The ability to CO arrest and phenotypically differentiate in response to RA were both grossly impaired. Unlike wild type cells which undergo early down-regulation and then hypophosphorylation of the RE protein when induced to differentiate, in resistant cells, hypophosphorylation of RE in response to NaB was grossly retarded. These changes in RE protein occurred faster when the cells were treated with VD3. In contrast, the changes in RB phosphorylation occurred significantly slower when the cells were treated with RA. The results suggest a coupling between the ability to GO growth arrest and phenotypically convert and the ability to hypophosphorylate RE. (C) 1995 Wiley-Liss, Inc.
引用
收藏
页码:502 / 509
页数:8
相关论文
共 32 条
[1]  
Breitman T.R., Selonick S.E., Collins S.J., Induction of differentiation of human promyelocytic leukemia cells (HL‐60) by retinoic acid, Proc Nat Acad Sci, 77, pp. 2936-2940, (1980)
[2]  
Collins S.J., Gallo R.C., Gallagher R.E., Continuous growth and differentiation of human myeloid leukemia cells in suspension culture, Nature, 270, pp. 347-349, (1977)
[3]  
Collins S.J., Bodner A., Ting R., Gallo R.C., Induction of morphological and functional differentiation of HL‐60 cells by compounds which induce differentiation in murine leukemia cells, Int J Cancer, 25, pp. 218-312, (1980)
[4]  
Gianni M., Zanotta S., Terao M., Garattini S., Garattini E., Effects of synthetic retinoids and retinoic acid isomers on the expression of alkaline phosphatase in F9 teratocarcinoma cells, Biochemical and Biophysical Research Communications, 196, pp. 252-259, (1993)
[5]  
Goldstein B., Kindregan H., Niles R.M., Effects of growth medium and cyclic AMP analogues on the cAMP‐induced differentiation of F9 teratocarcinoma cells, In Vitro Cell Develop Biol, 27 A, pp. 158-162, (1991)
[6]  
Huggenvik J.I., Collard M.W., Kim Y.W., Sharma R.P., Modification of the retinoic acid signaling pathway by the catalytic subunit of protein kinase‐A, Mol Endocrinol, 7, pp. 543-550, (1993)
[7]  
Inaba M., Okuno S., Koyama H., Nishizawa Y., Morii H., Dibutyryl cAMP enhances the effect of 1,25‐dihydroxy vitamin D3 on a human promyelocytic leukemia cell, HL‐60 at both the receptor and the postreceptor steps, Arch Biochem Biophys, 293, pp. 181-186, (1992)
[8]  
Jurutka P.W., Hsieh J.C., Haussler M.R., Phosphorylation of the human 1,25‐dihydroxy vitamin D3 receptor by cAMP‐dependent protein kinase, in vitro, and in transfected COS‐7 cells, Biochem Biophys Res Commun, 191, pp. 1089-1096, (1993)
[9]  
Krishnan A.V., Feldman D., Cyclic adenosine 3′ and 51‐monophosphate up‐regulates 1,25‐dihydroxy vitamin D3 receptor gene expression and enhances hormone action, Mol Endocrinol, 6, pp. 198-206, (1992)
[10]  
Kruyt F.A., Folkers G.E., Walhout A.J., van der Leede B.J., van der Saag P.T., E1A functions as a coactivator of retinoic acid‐dependent retinoic acid receptor‐beta 2 promoter activation, Mol Endocrinol, 7, pp. 604-615